Person: ÇETİNEL, ŞULE
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ÇETİNEL
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ŞULE
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Publication Metadata only Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice(ELSEVIER SCIENCE BV, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Sener, GokselThe protective effect of beta-glucan against oxidative injury caused by acetaminophen was studied in mice liver. BALB-c mice (25-30 g) were pretreated with beta-D-glucan (50 mg/kg, p.o.) for 10 days and on the 11th day they received an overdose of acetaminophen (900 mg/kg, i.p.). Four hours after the acetaminophen injection, mice were decapitated and their blood was taken to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels. Tissue samples of the liver were taken for histological examination or for the determination of levels of malondialdehyde, an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase activity, an index of tissue neutrophil infiltration. The formation of reactive oxygen species in hepatic tissue samples was monitored by using the chemilummescence technique with luminol and lucigenin probes. Acetaminophen caused a significant decrease in the GSH level of the tissue, which was accompanied with significant increases in the hepatic luminol and lucigenin chemiluminescence values, malondialdehyde level, MPO activity and collagen content. Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. On the other hand, P-D-glucan treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by acetaminophen. In conclusion, these results suggest that beta-D-glucan exerts cytoprotective effects against oxidative injury through its antioxidant properties and may be of therapeutic use in preventing acetaminophen toxicity. (c) 2006 Elsevier B.V. All rights reserved.Publication Metadata only Protective effects of resveratrol against acetaminophen-induced toxicity in mice(WILEY, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, Goksel; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Gedik, NursalThis investigation elucidates the role of free radicals in acetaminophen (AA)-induced toxicity and the possible protection by resveratrol (RVT). BALB-c mice were injected with a single dose of 900 mg/kg AA to induce toxicity, while RVT administred in a dose of 30 mg/kg i.p. following AA. Mice were sacrificed 4 h after AA injection to determine serum ALT, AST and tumor necrosis factor-alpha (TNF-alpha) levels in blood, and glutathione (GSH), malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity and collagen contents in liver tissues. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probe. ALT, AST levels and TNF-alpha were increased significantly after AA treatment, and reduced with RVT. AA caused a significant decrease in GSH levels while MDA levels and MPO activity were increased in liver tissues. On the other hand when RVT administered following AA, depletion of GSH and accumulation of MDA and neutrophil infiltration were reversed back to control. Furthermore increased luminol and lucigenin CL levels in the AA group reduced by RVT treatment. Our results implicate that AA causes oxidative damage in hepatic tissues and RVT, by its potent antioxidant effects protects the liver tissue. These data suggest that RVT may be of therapeutic use in preventing hepatic oxidative injury due to AA toxicity. (c) 2006 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only Ginkgo biloba extract ameliorates ischemia reperfusion-induced renal injury in rats(ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD, 2005) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, G; Sener, E; Sehirli, O; Ogunc, AV; Cetinel, S; Gedik, N; Sakarcan, AThere is increasing evidence to suggest that reactive oxygen metabolites (ROMs) play a role in the pathogenesis of ischemia/reperfusion injury (I/R) in the kidney. This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) on renal ischemia/reperfusion (I/R) injury. Wistar albino rats were unilaterally nephrectomized, and 15 days later they were subjected to 45 min of renal pedicle occlusion followed by 6h of reperfusion. Ginkgo biloba extract (EGb) (50mg kg(-1) day(-1)) or saline was administered twice, 15 min prior to ischemia and immediately before the reperfusion period. At the end of the treatment period, all rats were decapitated. Kidney samples were taken for histological examination or detennination of the renal malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Production of reactive oxidants was monitored by chemiluminescence (CL) assay. Creatinine and urea concentrations in blood were measured for the evaluation of renal function. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) were also assayed in serum samples. Ischemia/reperfusion caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity and collagen content of kidney tissues. Similarly, serum BUN and creatinine levels, as well as LDH and TNF-alpha, were elevated in the I/R group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by I/R. The findings imply that ROMs play a causal role in I/R-induced renal injury and EGb exerts renoprotective effects probably by the radical scavenging and antioxidant activities. (c) 2005 Elsevier Ltd. All rights reserved.Publication Open Access The protective effect of spironolactone and role of the Na+/K+-ATPase pump on intestinal ischemia/reperfusion injury(MARMARA UNIV, 2018-07-02) VELİOĞLU ÖĞÜNÇ, AYLİZ; Akyuz, Cebrail; Uzun, Orhan; Sunamak, Oguzhan; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Sehirli, Ahmet OzerThe aim of this study was to evaluate the possible protective effect of spironolactone (SPL) and role of the Na-K ATPase pump on intestinal ischemia/reperfusion injury. In our study, the period of ischemia was established by clamping the mesenteric artery for 45 minunder anesthesia in Wistar albino rats and the animals left for reperfusion at the end of this period were decapitated after one hour. Spironolactone (20 mg kg(-1)) was administered orally for three days before ischemia, 30 minbefore ischemia. The control group rats were subjected to the Sham operation and administered saline solution. TNF-alpha and IL-1 beta levels were measured in the serum samples. Ileal Na+/K+-ATPase, myeloperoxidase (MPO) analysis were performed. Structural injury was assessed histopathologically. Ischemia/reperfusion increased serum TNF-alpha and IL-1 beta levels together with MPO activity, whereas these values were maintained at the control group levels through SPL activation. However, ischemia/reperfusion decreased Na+/K+-ATPase activity in ileal tissues; however, these parameters were found to be significantly increased with SPL activation. The protective effect of SPL against ischemia/reperfusion injury by different mechanisms, mainly the activity of the Na+/K+-ATPase pump, suggests that this nontoxic agent may constitute a new clinical therapeutic principle.Publication Metadata only Resveratrol improves ifosfamide-induced Fanconi syndrome in rats(ACADEMIC PRESS INC ELSEVIER SCIENCE, 2007) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sehirli, Ozer; Sakarcan, Abdullah; Velioglu-Oeguenc, Ayliz; Cetinel, Sule; Gedik, Nursal; Yegen, Berrak C.; Sener, GoekselRegarding the mechanisms of ifosfamide (IFO)-induced urinary toxicity, several hypotheses have been put forward, among which oxidative stress and depletion of glutathione are suggested. This investigation elucidates the role of free radicals in IFO-induced toxicity and the protection by resveratrol, a natural phytoalexin. Wistar albino rats were injected intraperioneally with saline (0.9% NaCl; control), saline+ resveratrol (RVT; 10 mg/kg/day), ifosfamide (IFO; 50 mg/kg/day) or IFO+RVT for 5 days. Urine was collected for 24 h during the 5th day, and at the 120th h after the first injections, annuals were killed by decapitation and trunk blood was collected. Lactate dehydrogenase (LDH) activity, total antioxidant capacity (AOC) and pro-inflammatory cytokines TNF-alpha, IL-beta and IL-6 were assayed in plasma samples. Kidney and bladder tissues were obtained for biochemical and histological analysis. Formation of reactive oxygen species in the tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. The results demonstrated that IFO induced a Fanconi syndrome characterized by increased urinary sodium, phosphate, glucose and protein, along with increased serum creatinine and urea levels. On the other hand, RVT markedly ameliorated the severity of renal dysfunction induced by IFO. Furthermore IFO caused a significant decrease in plasma AOC. which was accompanied with significant increases in the levels of the pro-inflammatory mediators and LDH activity, while RVT treatment reversed all these biochemical indices. In the saline-treated IFO group, glutathione levels were decreased significantly, while the malondialdehyde levels, myeloperoxidase activity and collagen content were increased in both tissues, which were in parallel with the increases in CL values. In the RVT-treated IFO group, all of these oxidant responses were prevented significantly. Our results suggest that IFO causes oxidative damage in the renal and bladder tissues and resveratrol, via its antioxidant effects, protects these tissues. Therefore, its therapeutic role in proventing the development of chemotherapeutic drug-induced major toxicity in the urinary system requires further elucidation. (c) 2007 Elsevier Inc. All rights reserved.Publication Metadata only Meloxicam Exerts Neuroprotection on Spinal Cord Trauma in Rats(INFORMA HEALTHCARE, 2011) VELİOĞLU ÖĞÜNÇ, AYLİZ; Hakan, Tayfun; Toklu, Hale Zerrin; Biber, Necat; Celik, Hasan; Erzik, Can; Ogunc, Ayliz Velioglu; Cetinel, Sule; Sener, GokselTraumatic injury to the central nervous system results in the delayed dysfunction and neuronal death. Impaired mitochondrial function, generation of reactive oxygen species (ROS), and lipid peroxidation occur soon after traumatic spinal cord injury (SCI), while the activation of compensatory molecules that neutralize ROS occurs at later time points. The aim of the current study was to investigate the putative neuroprotective effect of the COX2 inhibitor meloxicam in a rat model of SCI. In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10, was used. Injured animals were given either 2 mg/kg meloxicam or saline 30 min postinjury by intraperitoneal injection. At seven days postinjury, neurological examination was performed and rats were decapitated. Spinal cord samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and DNA fragmentation. Formation of ROS in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique. SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in CL, MDA levels, MPO activity, and DNA damage. On the other hand, meloxicam treatment reversed all these biochemical parameters as well as SCI-induced histopathological alterations. Furthermore, impairment of the neurological functions due to SCI was improved by meloxicam treatment. The present study suggests that meloxicam, reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, GSH depletion, and DNA fragmentation.Publication Open Access Neuroprotective Effects of Alpha-Lipoic Acid in Experimental Spinal Cord Injury in Rats(TAYLOR & FRANCIS LTD, 2010-01) VELİOĞLU ÖĞÜNÇ, AYLİZ; Toklu, Hale Z.; Hakan, Tayfun; Celik, Hasan; Biber, Necat; Erzik, Can; Ogunc, Ayliz V.; Akakin, Dilek; Cikler, Esra; Cetinel, Sule; Ersahin, Mehmet; Sener, GokselBackground: Oxidative stress is a mediator of secondary injury to the spinal cord following trauma. Objective: To investigate the putative neuroprotective effect of a-lipoic acid (LA), a powerful antioxidant, in a rat model of spinal cord injury (SCI). Methods: Wistar albino rats were divided as control, vehicle-treated SCI, and LA-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10 was used. Injured animals were given either 50 mg/kg LA or saline at 30 minutes postinjury by intraperitoneal injection. At 7 days postinjury, neurologic examination was performed, and rats were decapitated. Spinal cord samples were taken for histologic examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and DNA fragmentation. Formation of reactive oxygen species in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique. Results: SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in luminol CL and MDA levels, MPO activity, and DNA damage. Furthermore, LA treatment reversed all these biochemical parameters as well as SO-induced histopathologic alterations. Conversely, impairment of the neurologic function caused by SCI remained unchanged. Conclusion: The present study suggests that LA reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, glutathione depletion, and DNA fragmentation.